Participation of ventral and dorsal tail muscles in bending movements of rat tail

The rat controls the form of its tail, from straight to curved, by contraction and relaxation of its four tail muscles. The tendons of these muscles insert on any of the cranial articular, transverse, and hemal processes of each of 24 coccygeal vertebrae (Co5–Co28). In this study, we isolated for the four coccygeal muscles each muscular fascicle segment inserting on any process of the coccygeal vertebrae. We measured the length and weight of all muscular fascicles and tendons, and then divided all muscular fascicles into four groups based on their insertion: Co5–Co10, Co11–Co16, Co17–Co22, and Co23–Co28. Moreover, we used soft X-ray imaging to investigate the geometrical relationship between neighboring coccygeal vertebrae. Additionally we carried out serial sectioning at the sacral and caudal portions, and traced the course of the tendons of coccygeal muscles from their origin to the Co4 level. We discuss which muscles and tendons play important roles when coccygeal vertebrae bend along and rotate around the longitudinal axis.     

Lack of effects for dietary exposure of bisphenol A during in utero and lactational periods on reproductive development in rat offspring

The potential for health effects on humans with exposure to bisphenol A (BPA) has raised concerns, and the adverse effects of low-dose exposure to BPA on reproduction have been controversial. The purpose of the present study was to investigate the effects of low-dose exposure to BPA on reproductive development in F(1) rat offspring. Pregnant female Sprague-Dawley rats (F(0)) were fed a diet containing low doses of BPA (0, 0.33, 3.3, or 33 ppm) from gestational day (GD) 6 through postnatal day (PND) 21. The weanlings (F(1)) from all dose groups were fed a normal diet ad libitum after weaning and then were subjected to necropsy at 5 weeks or 3 months of age. No BPA-related changes were observed in body weight or weight of any of the major reproductive organs in F(1) males and females. Epididymis weight was significantly lower only in 3-month-old F(1) males exposed to 33 ppm BPA. Anogenital distance (AGD), the ratio of AGD to the cube root of body weight, and relative ovary weight were significantly lower in 5-week-old F(1) females exposed to 3.3 and 33 ppm BPA, but significant differences were not observed in 3-month-old females. There were no BPA-related effects on cauda epididymal sperm motility in 3-month-old F(1) males. Plasma reproductive steroid hormone concentrations were not altered among groups in either sex. These outcomes indicate that low-dose exposure to BPA in the diet does not adversely affect reproductive development in F(1) rat offspring.     

From the position of a private sector hospital: ISO 15189 acquisition by a clinical laboratory, and quality management system deployment in the whole hospital

St. Mary's Hospital Medical Inspecting Center acquired ISO 15189 authorization in December, 2007. In the process of authorization acquisition, measures were taken to improve various quality issues, and a marked effect was seen in patient services and medical safety control. Furthermore, we tried to improve ward nursing management using ISO, drew up standard operating procedures through detailed job analysis, and enabled ward operation standardization. In this paper, while describing the effect of ISO 15189 on clinical examinations, we refer to the significance of improving quality of hospital management which our clinical laboratory lead to.     

Azithromycin suppresses proliferation, interleukin production and mitogen-activated protein kinases in human peripheral-blood mononuclear cells stimulated with bacterial superantigen

Objectives Macrolide antibiotics are used for the treatment of immunological disorders such as psoriasis. However, few studies have investigated the immunoregulatory efficacy of macrolides in bacterial superantigen‐stimulated immune cells. Methods The suppressive efficacies of azithromycin, clarithromycin, roxithromycin and prednisolone were evaluated in vitro against the concanavalin A‐ or toxic shock syndrome toxin 1 (TSST‐1)‐induced proliferation of peripheral‐blood mononuclear cells (PBMCs) obtained from nine healthy subjects. The concentrations of six cytokines in a PBMC‐culture medium were measured using bead‐array procedures followed by flow cytometry. Cellular c‐jun N‐terminal kinase (JNK) and extracellular signal‐regulated kinase (ERK) activity were measured using cell‐based ELISA procedures. Key findings Azithromycin, clarithromycin and roxithromycin inhibited the proliferation of both the concanavalin A‐ and superantigen‐stimulated PBMCs dose‐dependently. The effect of azithromycin was the strongest, with IC50 values of less than 5 µg/ml. Furthermore, the suppressive efficacy of prednisolone against concanavalin A‐ or TSST‐1‐stimulated PBMCs was significantly promoted in combination with 5 µg/ml azithromycin (P < 0.002). The concentrations of TNF‐α, interleukin (IL)‐2, ?4, ?5 and ?10 in the supernatant of concanavalin A‐ or TSST‐1‐stimulated PBMCs cultured for 72 h decreased by 65–98% in the presence of 5 µg/ml azithromycin. The stimulation of PBMCs with concanavalin A or TSST‐1 increased cellular JNK and ERK activity, and 5 µg/ml azithromycin significantly attenuated the increased activity of JNK in the TSST‐1‐stimulated cells and ERK in the concanavalin A‐ and TSST‐1‐stimulated PBMCs, respectively (P < 0.05). Conclusions Azithromycin suppresses mitogen‐ or superantigen‐induced proliferation of PBMCs by possibly inhibiting both cellular JNK and ERK activity.     

A high-fat diet inhibits the progression of diabetes mellitus in type 2 diabetic rats

It is well known that rats and mice, when fed a high-fat diet, develop obesity associated with abnormal glycolipid metabolism. In this study, we investigated the effects of a high-fat diet on a diabetic rat model, Spontaneously Diabetic Torii (SDT), which develops diabetes due to decreased insulin production and secretion with age. We hypothesized that a high-fat diet would accelerate the induction of diabetes in this model. The SDT rats were divided into 2 groups, which were fed a high-fat diet or standard diet for 16 weeks. The group fed a high-fat diet developed obesity, hyperinsulinemia, and hyperlipidemia until 16 weeks of age. Before 16 weeks of age, hyperglycemia accompanied by hypoinsulinemia developed in the group on a standard diet, but serum glucose levels were comparable in both groups. After 16 weeks of age, the group on a standard diet showed an increase in serum glucose levels and a decrease in serum insulin levels. Unexpectedly, in the group on the high-fat diet, we observed a suppressed of the progression of hyperglycemia/hypoinsulinemia. Histopathological observation revealed more pancreatic beta cells in the group on the high-fat diet. This study suggests that feeding SDT rats a high-fat diet induces obesity, hyperinsulinemia, and hyperlipidemia, but not hyperglycemia, until 16 weeks of age. Thereafter, age-dependent progress of hyperglycemia and hypoinsulinemia was delayed by a high-fat diet. The hyperfunction of pancreatic beta cells induced by a high-fat diet before the onset of hyperglycemia appears to suppress development of hyperglycemia/hypoinsulinemia.     

Gene expression analyses on embryonic external genitalia: identification of regulatory genes possibly involved in masculinization processes

Androgen plays a crucial role in initiating and maintaining the expression of male sexual characteristics in mammals. In humans and mice, any defects along the pathway of androgen functions result in congenital urogenital abnormalities. The genital tubercle (GT), an anlage of the external genitalia, differentiates into a penis in males and a clitoris in females. Although masculinization of the external genitalia is androgen-dependent, the molecular pathway of its potential downstream genes is largely unclear. To identify the genes involved in mouse GT masculinization, we performed gene expression analyses, such as real-time quantitative polymerase chain reaction and section in situ hybridization analysis. From our studies we have identified candidate genes, Cyp1b1, Fkbp51 and MafB as potential androgen targets during mouse GT masculinization.     

Anti‐inflammatory effects of caffeic acid phenethyl ester (CAPE), a nuclear factor‐κB inhibitor,on Helicobacter pylori‐induced gastritis in Mongolian gerbils

Nuclear factor‐κB (NF‐κB) plays a major role in host inflammatory responses and carcinogenesis and as such is an important drug target for adjuvant therapy. In this study, we examined the effect of caffeic acid phenethyl ester (CAPE), an NF‐κB inhibitor, on Helicobacter pylori (H. pylori)‐induced NF‐κB activation in cell culture and chronic gastritis in Mongolian gerbils. In AGS gastric cancer cells, CAPE significantly inhibited H. pylori‐stimulated NF‐κB activation and mRNA expression of several inflammatory factors in a dose‐dependent manner, and prevented degradation of IκB‐α and phosphorylation of p65 subunit. To evaluate the effects of CAPE on H. pylori‐induced gastritis, specific pathogen‐free male, 6‐week‐old Mongolian gerbils were intragastrically inoculated with H. pylori, fed diets containing CAPE (0–0.1%) and sacrificed after 12 weeks. Infiltration of neutrophils and mononuclear cells and expression of NF‐κB p50 subunit and phospho‐IκB‐α were significantly suppressed by 0.1% CAPE treatment in the antrum of H. pylori‐infected gerbils. Labeling indices for 5′‐bromo‐2′‐deoxyuridine both in the antrum and corpus and lengths of isolated pyloric glands were also markedly reduced at the highest dose, suggesting a preventive effect of CAPE on epithelial proliferation. Furthermore, in the pyloric mucosa, mRNA expression of inflammatory mediators including tumor necrosis factor‐α, interferon‐γ, interleukin (IL)‐2, IL‐6, KC (IL‐8 homologue), and inducible nitric oxide synthase was significantly reduced. These results suggest that CAPE has inhibitory effects on H. pylori‐induced gastritis in Mongolian gerbils through the suppression of NF‐κB activation, and may thus have potential for prevention and therapy of H. pylori‐associated gastric disorders. © 2009 UICC